The Brattleboro strain of rats suffers from a genetically based defect that results in lack of the hormone vasopressin (VP) with consequent diabetes insipidus (DI). Earlier research findings have established that these genetically VP-deficient rats, in addition to DI, suffer altered memory function. Exogenous VP not only relieves their DI symptoms, it also improves memory. Recently, it has been found in some instances that transplants of fetal brain tissue containing VP-producing neurons can integrate with the host's brain with consequent amelioration of Brattleboro rats' DI symptoms. This project has five specific aims: (1) by behavioral tests to characterize more adequately the nondrinking behavioral symptoms that are associated with VP deficiency; (2) to evaluate effectiveness of chronically infused VP in Brattleboro rats on nondrinking behavior; (3) to test the hypothesis that the behavioral defect in Brattleboro rats is a consequence of their characteristically heightened oxytocin levels (OT) by studying the behavioral effect of OT infusions in normal rats; (4) to elucidate some possible neurochemical mechanisms that underlie the nondrinking behavioral impairments of Brattleboro rats by investigating catecholamine metabolism; and (5) to provide appropriate behavioral tests of Brattleboro rats that have received transplants of fetal VP-producting neurons to determine if the consequent changes in DI symptoms are also associated with improved performance of nondrinking behavior. Besides its intrinsic scientific interest, this latter problem could well be an important step in the development of treatment for some neurological disorders by neural transplants.